Field of the Invention
The present invention relates generally to the field of systems and methods for partitioning body conduits with a class of prosthetic partitioning devices, specifically with prosthetic devices for placement in and/or about pulmonary vein(s) for the purpose of treating congestive heart failure, to procedures for installing same.
Background of the Invention
Congestive heart failure is a complex syndrome of various etiologies associated, in some patients, with abnormally high pulmonary venous pressures at rest and/or in conjunction with physical, emotional or metabolic stress. Congestive heart failure is a major cause of cardiovascular morbidity and mortality, affecting tens of millions of patients worldwide. Current treatment of chronic congestive heart failure often relies on life-long medical therapy if congestive heart failure persists after correction of all reversible causes of congestive heart failure.
As illustrated in FIG. 1, the left atrium LA of the human heart H receives oxygenated blood from the lungs (not shown) through the pulmonary veins PV (the right and left superior and inferior pulmonary veins), and delivers it through the mitral MV to the left ventricle LV. Contraction of the left ventricle LV pumps the oxygenated blood across the aortic valve AV into the high pressure, high resistance systemic circulation through the aorta A, and out to the rest of the body (See general flow direction as indicated by arrow F in FIG. 1).
For the purposes of illustration, the anatomy of central larger pulmonary veins is compared with anatomy of larger veins in the lower extremities in humans. Certain larger veins in the lower extremities of human beings normally have valves that, under conditions of normal function, permit movement of blood largely only toward the heart. In effect, properly functioning venous valves in the lower extremities protect, or partition, the veins of the lower extremities from the relatively high hydrostatic pressure of the column of venous blood between the right atrium RA and the lower extremities due to the effect of gravity during upright posture. Thus, normally, when upright posture is assumed, venous blood pressure in the foot is predominantly less than the sum of relatively low pressure in the right atrium RA and relatively high hydrostatic pressure of the column of venous blood between the right atrium RA and the foot due to the effect of gravity. When these venous valves in the lower extremities are incompetent, venous blood pressure in the foot becomes predominantly equal to the sum of the relatively low pressure in the right atrium RA and relatively high hydrostatic pressure of the column of venous blood between the right atrium RA and the foot, often resulting in pathologic dilatation of the veins in the lower extremities and/or edema.
The pulmonary veins PV, which drain into the left atrium LA, are not known to have directional valves in humans or other mammals. Under normal conditions, the pressure in the pulmonary veins PV is, with a phase shift dependent on the distance from the left atrium LA, essentially the same as or slightly higher than the pressure in the left atrium LA. Thus, protection, or partitioning, of the pulmonary veins PV from the high systolic pressure of the contracting left ventricle LV, is the same as the protection of the left atrium LA. Such protection is entirely and solely due to proper function of the mitral valve MV. An example of abnormal function of the mitral valve MV is mitral regurgitation, in which insufficient closure of the mitral valve MV allows the systolic flow of blood from the left ventricle LV into the left atrium LA. The mitral regurgitation may occur due to damage or malfunction of the mitral valve leaflets, and/or the mitral annulus, and/or the chordae tendineae, and/or the papillary muscles, and/or dilatation of the left ventricle LV. During systole, the impaired partitioning of the left ventricle LV from the left atrium LV, and therefore from the pulmonary veins PV, transmits relatively high left ventricular systolic pressure, with a phase shift, into the pulmonary veins PV, which often results in marked elevation of the mean pulmonary venous pressure PV, and leading to pulmonary edema and congestive heart failure. Another example of abnormal function of the mitral valve MV is mitral stenosis. In mitral stenosis, opening of the mitral valve MV in diastole and the normal diastolic blood flow from the left atrium LA into the left ventricle LV are compromised due to damage or malfunction of the mitral valve leaflets and chordae tendineae, and occur only at markedly elevated diastolic, and therefore mean, pressure in the left atrium LA. This elevated pressure is transmitted, with a phase shift, into the pulmonary veins PV, resulting in marked elevation of the mean pulmonary venous pressure PV. In patients with mitral stenosis (despite typically normal systolic function of the mitral valve MV providing effective systolic partitioning between the left ventricle LV and left atrium LA, and therefore pulmonary veins PV), signs and symptoms of congestive heart failure may develop due to markedly elevated diastolic, and therefore mean, pressure in the left atrium LA, and therefore pulmonary veins PV.
Treatment of congestive heart failure largely due to mitral regurgitation is typically often performed by surgical replacement of the mitral valve with a prosthetic valve. In a substantial number of patients, surgical replacement of a regurgitant mitral valve is not possible, or is associated with unacceptable high morbidity and/or mortality.
In other patients, the left ventricle LV may become non-compliant, or stiff, due to a variety of conditions such as, but not limited to, ischemic heart disease, hypertension, aortic stenosis, diabetes mellitus, or aging. The transfer of blood into a left ventricle LV having decreased compliance during diastole can only be effected when the left atrial, and therefore pulmonary venous, diastolic pressure is markedly elevated. In such patients, despite typically normal function of the mitral valve providing effective systolic partitioning between the left ventricle LV and left atrium LA, and therefore pulmonary veins PV, signs and symptoms of congestive heart failure may develop due to markedly elevated diastolic, and therefore mean, pressure in the left atrium LA, and therefore pulmonary veins PV. At present, congestive heart failure due to diastolic left ventricular dysfunction can only be treated with medications, with variable efficacy.
Accordingly, there is a need for a system that provides effective partitioning of the left atrium and pulmonary veins without the need for medications or valve replacement therapies.